Coronary Collateral Development In Patients Research Articles

Effect of Statin Treatment on Coronary Collateral Development in Patients With Diabetes Mellitus

Coronary collateral development is an important compensatory mechanism in advanced coronary artery disease, and patients with diabetes mellitus have impaired coronary collateral development. This study tested the hypothesis that statin treatment may increase coronary collateral development in patients with diabetes mellitus. The study population consisted of 149 consecutive diabetic patients who underwent clinically indicated coronary angiography and had >95% stenosis of > or =1 major coronary artery. Clinical information, including age, gender, history of hypertension, smoking, myocardial infarction, clinical presentation, and medications, was recorded before coronary angiography. Coronary collaterals were graded according to the Cohen-Rentrop method. Collateral grading was classified as poor when the collateral grade was 0 to 1 and good when it was 2 to 3. Among 149 patients (85 men; mean age 62 +/- 10 years), 74 (56%) were receiving statin treatment. In multivariate analysis, among demographic, clinical, and angiographic parameters, only statin therapy (odds ratio 3, 95% confidence interval 1.5 to 6.03, p = 0.002) and stable angina pectoris (odds ratio 3.24, 95% confidence interval 1.42 to 7.41, p = 0.005) were found to be independent predictors of better collateral formation. In conclusion, stable angina pectoris and statin treatment are associated with better coronary collateral development in patients with diabetes mellitus.

Obesity is associated with impaired coronary collateral vessel development

Chronic myocardial ischaemia due to coronary artery stenosis or occlusion has been shown to increase the growth of coronary collateral circulation. Collateralization leads to increased oxygen delivery to the area at risk and hence may reduce ischaemia, prevent infarction and preserve contractile function. However, there is considerable variation among patient subsets in terms of the presence or degree of collateralization. We aimed to evaluate the relationship between obesity and coronary collateral development in patients with ischaemic heart disease. In all, 215 patients (mean age, 57.8+/-8.9 y) with body mass index (BMI)> or =30 kg/m(2) were enrolled into our study. A total of 90 age- and sex-matched patients (mean age, 58.7+/-10 y) with BMI<25 kg/m(2) and significant coronary artery disease were selected as a control group. The mean age and distribution of risk factors for coronary heart disease were not significantly different between two groups other than poorer HDL cholesterol and triglyceride profile in obese patients. The mean BMI was significantly higher in the patient group (33.3+/-2.4 vs 22.8+/-1.7, P<0.001). The mean number of diseased vessels and maximum lesion severity were not significantly different between the two groups. The mean Rentrop collateral score of the patient group was significantly worse than the control group (1.08+/-0.68 vs 2.10+/-0.72, P<0.001). Our findings suggest that collateral vessel development is poorer in obese patients (defined as BMI> or =30 kg/m(2)) with ischemic heart disease compared to normal range BMI, and the risk of having poor collateral vessel development is significantly increased. However, this might be reflecting the cluster of risk factors, associated with metabolic syndrome, in which insulin resistance plays a major role.

Pericardial levels of the anti-angiogenic factor endostatin correlate with coronary collateral development in patients with ischemic heart disease

Pericardial levels of the anti-angiogenic factor endostatin correlate with coronary collateral development in patients with ischemic heart disease